BACKGROUND: We assessed the efficacy of aggressive lipid controlling therapy (ALCT), which maintains low-density lipoprotein cholesterol (LDL-C) below to 80 mg/dL and LDL/high-density lipoprotein cholesterol (HDL-C) ratio less than 1.5 for preventing postcoronary bypass (CABG) saphenous vein graft (SVG) diseases by using intracoronary angioscopy. METHODS:Twenty-one patients after CABG were divided into two groups: group I consisted of 10 patients whose serum LDL-C level and LDL/HDL could be controlled less than 80 mg/dL and 1.5, respectively, by rosuvastatin for about one year; group II consisted of 11 patients whose LDL-C level and LDL/HDL have been higher than 100 mg/dL and 2.5, respectively, regardless of having medication of pravastatin. Twenty-seven SVGs were assessed by intravascular ultrasound (IVUS) and angioscopy on postoperative 12 to 16 months. RESULTS: The serum LDL-C level (I: 64.1 vs II: 130.2 mg/dL) and LDL/HDL (I: 1.36 vs II: 2.64), and high sensitive C-reactive protein (I: 0.045 +/- 0.100 vs II: 0.116 +/- 0.020 mg/dL) were significantly lower in group I. In group II, IVUS detected eccentric plaques in 11 (78.6%) of 14 SVGs. Furthermore the angioscope showed yellow plaque in all 14 SVGs (100%) and 11 (78.6%) of them had thrombi. On the other hand, in group I, all 13 SVGs had no eccentric, yellow plaques or thrombi and the intima was entirely clear white. CONCLUSIONS: Prophylactic treatment for yellow plaque and thrombus formation are extremely important in the development of early and late SVG disease. Aggressive lipid controlling therapy is quite attractive to avoid post CABG SVG disease and may be effective to maintain the long-term graft patency.
RCT Entities:
BACKGROUND: We assessed the efficacy of aggressive lipid controlling therapy (ALCT), which maintains low-density lipoprotein cholesterol (LDL-C) below to 80 mg/dL and LDL/high-density lipoprotein cholesterol (HDL-C) ratio less than 1.5 for preventing postcoronary bypass (CABG) saphenous vein graft (SVG) diseases by using intracoronary angioscopy. METHODS: Twenty-one patients after CABG were divided into two groups: group I consisted of 10 patients whose serum LDL-C level and LDL/HDL could be controlled less than 80 mg/dL and 1.5, respectively, by rosuvastatin for about one year; group II consisted of 11 patients whose LDL-C level and LDL/HDL have been higher than 100 mg/dL and 2.5, respectively, regardless of having medication of pravastatin. Twenty-seven SVGs were assessed by intravascular ultrasound (IVUS) and angioscopy on postoperative 12 to 16 months. RESULTS: The serum LDL-C level (I: 64.1 vs II: 130.2 mg/dL) and LDL/HDL (I: 1.36 vs II: 2.64), and high sensitive C-reactive protein (I: 0.045 +/- 0.100 vs II: 0.116 +/- 0.020 mg/dL) were significantly lower in group I. In group II, IVUS detected eccentric plaques in 11 (78.6%) of 14 SVGs. Furthermore the angioscope showed yellow plaque in all 14 SVGs (100%) and 11 (78.6%) of them had thrombi. On the other hand, in group I, all 13 SVGs had no eccentric, yellow plaques or thrombi and the intima was entirely clear white. CONCLUSIONS: Prophylactic treatment for yellow plaque and thrombus formation are extremely important in the development of early and late SVG disease. Aggressive lipid controlling therapy is quite attractive to avoid post CABG SVG disease and may be effective to maintain the long-term graft patency.